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Tim Hackett, DVM, MS and Wayne E. Wingfield, DVM, MS 1. What groups of poisonous snakes cause the most problems for domestic animals in the United States? There are 3 groups of poisonous snakes in the U.S.  Pit Vipers are the largest group and include rattlesnakes, copperheads, and water moccasins.  Pit vipers have theremoreceptor organs ("pits") between the eye and nostril, triangular-shaped heads, and retractable fangs.
  Elapids. include coral snakes. They are brightly colored and have fixed fangs. The coloring of coral snakes differentiates them from the similar but harmless king snake:
Rescuers should be careful not to get bitten. The best treatment for rattlesnake envenomation is to take the animal to a veterinary hospital as soon as possible. Tourniquets, suction devices and local application of electrical current have been reports for early management of rattlesnake envonomation. These intervents may delay transport, and non has proved efficacious. 3. What are the common clinical signs associated with pit viper attack? "Snakebite" can be difficult to diagnose. In general, pit viper envenomation produces a local reaction. Look for fang marks, rapid swelling, edema and pain at the site. Other symptoms may include erythema, petechia, ecchymosis and tissue necrosis. Clinical signs of systemic illness include vomiting, respiratory distress, tachycardia or arrhythmia, hypotension, bleeding disorders, mystagmus and fever. 4. Once the animal arrives at the hospital, how can you determine whether the animal was envenomated by a rattlesnake? Owners may present their animals after coming in close contact with a rattlesnake, unsure whether the animal was bitten. If envenomation has occurred, the affected areas usually develop marked edema and erythema within 1 hour of the strike. The face, neck and forelimbs should be examined care fully for fang marks, swelling and bleeding; the animal may be in extreme pain. Measurement of swollen areas should be repeated, because rapid swelling indicates probable snakebite. One useful test for envenomation is to examine a peripheral blood smear for echinocytes. 5. How do you examine for echinocytes? What do they look like? A drop of the patient's blood is placed on a slide with a drop of saline and examined under the microscope for echinocytosis. Small, finely crenated echinocytes are present and affect most of the red blood cells. Often this change is seen before swelling and systemic illness become apparent. As you monitor the peripheral blood smear, the number of echinocytes decreases each day; by day 3-5, it is nearly impossible to find these abnormal cells. the mechanism of echinocytosis is unknown in envenomation but probably involves uncoupling of oxidative metabolism. In addition, dogs bitten by rattlesnakes do not have increased levels of bilirubin, as one may expect if the echinocytes were destroyed by the spleen. For some reason, perhaps because of massive tissue injury by envenomation, dogs often show increased fractional excretion of potassium in the urine. 6. What determines the severity of a snakebite? Many factors influence the amount and type of venom received and the host's reaction. Host size and health are important, as are regional and species differences among snakes. Bits from copperheads and prairir rattlesnakes are usually minimally symptomatic. Conversely, in some southwestern desert areas the Mojave rattlesnake may cause respirtatory paralysis and rapid death. The age and size of the snake, time of day, time since the snake's last meal, and season affect the amount of venom administered in a bite. Many biest are dry and nonpoisonous. They may be painful but usually show no signs of swelling. Wounds still should be considered contaminated, and appropriate cleaning and antibiotic therapy are indicated. 7. What is a dry snakebite? A dry snakebite is present if no venom is realeased at the time of the bite. Clinically a dry snakebite is assumed if no pain or swelling occurs within 1 hour of envenomation. 8. What toxic components are found in pit viper venoms? Rattlesnake venom contains various proteolytic enzymes. An early, direct effect of an enzyme called kininogenase is bradykinin activation. Bradykinin is a potent vasodilator on its own, but it also stimulates endogenous phospholipase A, which stimulates the arachidonic cascade to produce various inflammatory eicosanoids, including prostaglandins I2, E2 and thromboxane A2. The results are systemic inflammation, vasodilation, and severe hypotension. Rattlesnake venom also distrupts the basal lamina and collagen of the capilaries, allowing leakage of blood cells and plasma into the surrounding tissues. Signs include edema and petechia. Venom may cause platelet aggregation and margination through damage to the endothelium. Activated platelets then produce thromboxane and prostaglandins, which attract more platelets and white blood cells. Activation of platelets and the coagulation cascade may lead to consumption of clotting factors. The snake's venom also has a thrombinlike enzyme that cleaves fibrin and adds to the mechanisms of disseminated intravascular coagulation (DIC). 9. What are the first steps to treat snake envenomation? When an animal presents in distress after rattlesnake envenomation, the clinician should first assess the ABC's of resuscitation: A. Airway patency should be assessed. The airway may become obstructed if swelling and edema affect the face or throat. If necessary, the patient should be intubated or a tracheostomy performed. B. Breathing should be assessed by auscultation and examination of mucus membranes. C. Circulation is assessed by palpating pulses, auscultating the heart, and again assessing mucous membrane color and capillary refill. If possible, blood pressure also should be checked. Because the most serious early complication of rattlesnake bite is hypotension, a large-bore intravenous catheter should be placed and a balanced crystalloid solution started. Volumes and fluid rate should be based on clinical signs. In general, be prepared to give a whole blood volume (90 ml/kg in dogs) in the first hour. The patient's response to fluids should guide further therapy. Be aware of the potential fluid loss associated with increased capillary permeability. Patients presented within a few hours of a bite usually swell much more in the hospital. Continuous reassessment of vital functions is mandatory. Blood and urine should be collected for baseline data, coagulation testing and identification of early myoglobinuria. 10. When should antivenin be given? Rattlesnake antivenin is a polyvalent compound containing serum globulins from horses immunized with venoms of the major pit vipers (family: Crotalidae). Antivenin is contraindicated only in patients with known hypersensitivity. Unfortunately, there is no correlation between positive intradermal skin reactions and identification of early antivenin reactions. Normally, the antibodies in horse serum combine with the snake's venom to neutralize it. It may be life-saving in severely affected animals and limits the morbidity of relatively minor envenomation. Use of antivenin is controversial because many animals recover without it, it is expensive, and it is not without some risk of anaphylaxis. The dose may be quite variable. In people 2-4 vials are recommended for moderate envenomation (large swelling and abnormal laboratory tests) and up to 15 vials for severe envenomation (systemic manifestations). In animals, the number of vials depends on the severity of clinical signs, size of the patient, and the location of the bite (smaller patients and snakebites on the digits generally require 50% more antivenin than larger patients and nondigital bites). Routine antivenin therapy may be cost prohibitive. Mild envenomation may be reated successfully with supportive therapy alone. Clients should be informed or the potential benefit of antivenin and the possible need to give multiple doses. Antivenin administration should be monitored closely. If a patient shows signs of anaphylaxis, discontinue the antivenin and administer corticosteroids and epinephrine. 11. Is serum sickness a common complication of antivenin therapy? About 50-75% of humans who are given antivenin develop serum sickness, a type II hypersensitivity reactions that may occur up to 30 days after administration. Clinical signs in humans include lymphadenopathy, skin rashes, fever, and arthralgia. Evidence indicates that patients given systemic glucocorticoids have a significantly decreased risk for development of serum sickness. Serum sickness may not be a common complication in animals because of the expense of using several vials of antivenin. 12. Are any treatments contraindicated in patients with snakebite? Tourniquets are useful only if applied immediately and should not be used for head or neck wounds. Cold packs may delay the spread of venom but also can increase the amount of tissue damage. Electroshock therapy has been advocated to denature the protein constituents of venom. It is now believed that this treatment merely contributes to local tissue damage and should not be used. Patients with rhabdomyolysis and metabolic acidosis should not received lactated Ringer's solution. A non-lactate-containing buffered crystalloid solution should be used. Although hetastarch is a useful colloid to manage increased vascular permeability, it should not be used in patients with coagulopathies. 13. What complications should you anticipate? The proteolytic enzymes associated with rattlesnake venom may induce babdomyolysis and myoblobinuria. Myoglobin is nephrotoxic and renal failure is a potential complication. Intravenous fluid therapy and close attention to urine character and output should identify problems early. DIC is a common complication. Patients should be screened once or twice daily with activated clotting times. Blood smears identify schistocytes and laboratory evaluation of fibrin degradation products and antithrombin III identifies DIC. 14. How should you treat DIC associated with snakebite? DIC should be anticipated. Aggressive supportive care, including intravenous fluid therapy, helps to treat the primary problem, dilutes the toxin and enhances renal clearance. Antivenin may decrease the incidence of DIC but is most effective before serious complications develop. The use of fresh and fresh frozen plasma to provide clotting factors and antithrombin III can be augmented by incubating the plasma with heparin before administration. If severe anemia also develops, fresh whole blood also provides needed factors and can be incubated with heparin. |